Hyperhomocysteinaemia is an independent risk factor for CVD. Recent data show a relationship between homocysteine (Hcy) and free radical formation. Since creatine synthesis is responsible for most of the methyl group transfers that result in Hcy formation, creatine supplementation might inhibit Hcy production and reduce free radical formation. The present study investigated the effects of creatine supplementation on Hcy levels and lipid peroxidation biomarkers. Thirty rats were divided into three groups: control group; diet with creatine group (DCr; 2 % creatine in the diet for 28 d); creatine overload plus diet with creatine group (CrO+D; 5 g creatine/kg by oral administration for 5 d+2 % in the diet for 23 d). Plasma Hcy was significantly lower (P < 0·05) in DCr (7·5 (sd 1·2) μmol/l) and CrO+D (7·2 (sd 1·7) μmol/l) groups compared with the control group (12·4 (sd 2·2) μmol/l). Both plasma thiobarbituric acid-reactive species (TBARS) (control, 10 (sd 3·4); DCr, 4·9 (sd 0·7); CrO+D, 2·4 (sd 1) μmol/l) and plasma total glutathione (control, 4·3 (sd 1·9); DCr, 2·5 (sd 0·8); CrO+D, 1·8 (sd 0·5) μmol/l) were lower in the groups that received creatine (P < 0·05). In addition, Hcy showed significant negative correlation (P < 0·05) with plasma creatine (r − 0·61) and positive correlation with plasma TBARS (r 0·74). Plasma creatine was negatively correlated with plasma TBARS (r − 0·75) and total peroxide (r − 0·40). We conclude that creatine supplementation reduces plasma Hcy levels and lipid peroxidation biomarkers, suggesting a protective role against oxidative damage. Modulating Hcy formation may, however, influence glutathione synthesis and thereby affect the redox state of the cells.

Research has shown associations between attention-deficit/hyperactivity disorder (ADHD) and erythrocyte long-chain n-3 PUFA (LC n-3 PUFA) levels, with limited evidence for dietary LC n-3 PUFA intake and ADHD. The aims of the present study were to assess dietary PUFA intakes and food sources in children with ADHD, to compare these intakes to previously published Australian National Nutrition Survey (NNS) data and determine any relationships between intakes and ADHD symptoms. Eighty-six 3-d-weighed food records (FR) were analysed from children with ADHD. The median (interquartile range) daily intakes of fatty acids (mg/d) were: linoleic acid (18 : 2n-6), 7797 (6240–12 333); arachidonic acid (20 : 4n-6), 55 (27·0–93); total n-6 PUFA, 7818 (6286–10 662); α-linolenic acid (18 : 3n-3), 1039 (779–1461); EPA (20 : 5n-3), 18 (6·0–32·0); docosapentaenoic acid (22 : 5n-3), 17 (6·3–39·3); DHA (22 : 6n-3), 16 (8·5–445); total LC n-3 PUFA (addition of 20 : 5n-3, 22 : 5n-3 and 22 : 6n-3), 65 (28·3–120·1); total n-3 PUFA, 1151 (876–1592). In comparison to the NNS data, 18 : 3n-3 intakes were higher and 20 : 4n-6 were lower (P < 0·05). Children with ADHD consumed half the amount of fish/seafood, meat and eggs when compared to the NNS (P < 0·05). No significant correlations were found between fatty acids and ADHD symptoms. Children with ADHD met the adequate intake for LC n-3 PUFA, but fell short of other recommendations.

n-3 PUFA have well-recognised cardio-beneficial effects. In contrast, premature coronary deaths are associated with consumption of high levels of trans-fatty acids (TFA). The present study determined the effects of n-3 PUFA and TFA on sudden cardiac death and vascular inflammation. A rat coronary ligation model was used to study the effect of fatty acids on sudden cardiac death, whereas a mouse femoral artery ligation model was used to study compensatory vascular remodelling. Human aortic endothelial cells (HAEC) were utilised for the in vitro studies to investigate expression of inflammatory molecules. Feeding animals an n-3 PUFA-enriched diet caused a sevenfold increase in plasma n-3 PUFA compared with that of the TFA-fed group, whereas a TFA-enriched diet caused a 2·5-fold increase in plasma TFA compared with the n-3 PUFA group. Animals on a TFA diet had a lower survival rate due to sudden cardiac death and exhibited variable degrees of aortic atherosclerotic lesions. Animals on a TFA diet had diminished hindlimb collateral growth, whereas animals on the n-3 PUFA diet exhibited extensive collateral growth about ligated regions. HAEC treated with TFA (trans-18 : 2) showed significantly increased expression of intracellular adhesion molecule-1 and nitrosylation of cellular proteins than those treated with DHA (n-3 PUFA, 22 : 6). The in vivo study demonstrates that, in contrast to TFA, n-3 PUFA improve animal survival after myocardial infarction, prevent development of atherosclerotic lesions and stimulate compensatory vascular remodelling. The in vitro study demonstrates that TFA induce, while n-3 PUFA prevent, vascular inflammation.

Polycyclic aromatic hydrocarbons (PAH) are procarcinogens that can be commonly found in our food and environment. Upon biotransformation in our body system, they can cause DNA damage through the generation of genotoxic species and oxidative stress. Phase I and II enzymes are pivotal in the process of proximate carcinogen formation and elimination. Some dietary phytochemicals are strong inhibitors to the phase I enzymes. In the present study, we investigated the effect of the red wine compound resveratrol on DNA damage induced by PAH in a non-tumorigenic breast cell line MCF-10A. Resveratrol ranging from 1 to 5 μm could significantly suppress the expressions of cytochrome P450 (CYP) 1A1, CYP1B1 and UDP-glucuronosyltransferase (UGT) 1A1 induced by 7,12-dimethylbenz[a]anthracene (DMBA). The comet assay indicated that DMBA introduced DNA damage to these cells, and co-treatment of resveratrol at 5 or 10 μm could alleviate the damage. Further investigation illustrated that resveratrol reduced the binding of DMBA metabolites to DNA with no effect on DMBA-induced oxidative DNA damage. Since the phase II enzyme UGT1A1 was suppressed, the elimination of DMBA metabolites would not have contributed to the reduction in the DMBA metabolite–DNA binding. In summary, resveratrol might protect breast cells against PAH-induced DNA damage. The underlying mechanism was mediated by phase I enzyme suppression rather than phase II enzyme induction or oxidative DNA repair.

Both K and Ca supplementation may have beneficial effects on bone through separate mechanisms. K in the form of citrate or bicarbonate affects bone by neutralising the acid load caused by a high protein intake or a low intake of alkalising foods, i.e. fruits and vegetables. Ca is known to decrease serum parathyroid hormone (S-PTH) concentration and bone resorption. We compared the effects of calcium carbonate, calcium citrate and potassium citrate on markers of Ca and bone metabolism in young women. Twelve healthy women aged 22–30 years were randomised into four controlled 24 h study sessions, each subject serving as her own control. At the beginning of each session, subjects received a single dose of calcium carbonate, calcium citrate, potassium citrate or a placebo in randomised order. The diet during each session was identical, containing 300 mg Ca. Both the calcium carbonate and calcium citrate supplement contained 1000 mg Ca; the potassium citrate supplement contained 2250 mg K. Markers of Ca and bone metabolism were followed. Potassium citrate decreased the bone resorption marker (N-terminal telopeptide of type I collagen) and increased Ca retention relative to the control session. Both Ca supplements decreased S-PTH concentration. Ca supplements also decreased bone resorption relative to the control session, but this was significant only for calcium carbonate. No differences in bone formation marker (bone-specific alkaline phosphatase) were seen among the study sessions. The results suggest that potassium citrate has a positive effect on the resorption marker despite low Ca intake. Both Ca supplements were absorbed well and decreased S-PTH efficiently.

China is experiencing a rapid increase in overweight and related conditions. This study describes the geographic variation in BMI levels and the prevalence of overweight and underweight in Chinese adults, and assesses their relations with regional Gross Domestic Product (GDP) per capita levels. BMI values and the prevalence of overweight and underweight in 143 522 adults from the Chinese National Nutrition and Health Survey (2002) were calculated according to geographic regions in China. Their correlations with GDP were assessed. Linear and logistic regressions were used to adjust for age, sex and city–country composition. BMI and the prevalence of overweight were highest in the Bohai coastal regions while lowest in southern provinces such as Guangdong, Guangxi, Yunnan, Hunan and Fujian. Mean BMI values ranged from 20·72 to 25·48 kg/m2, and the prevalence of overweight ranged from 6·6 to 53·9 %. BMI and the prevalence of overweight were positively correlated with economic development, particularly in the northern regions. However, for regions with similar GDP per capita levels, those in the south had substantially lower BMI and lower prevalence of overweight than those in the north. Interestingly, some southern regions with high GDP per capita had low BMI and low prevalence of overweight. The prevalence of underweight was highest in the south. Substantial geographic variations in the prevalence of overweight and underweight exist in China. Such variations cannot be fully explained by the differences in economic status. China is currently facing challenges of both overweight and underweight but priorities vary in different regions.

The present experiment aimed to study the influence of six sources of non-digestible carbohydrates (NDC) on the mucous layer in the colon of rats. The NDC sources used were as follows: cellulose (C); pectin (P); inulin; resistant starch (RS); barley hulls. The diets contained 108–140 g NDC/kg DM. A fibre-free (FF) diet served as a control. The diets were fed to forty-eight rats for 34–41 d. The thickness of the total mucous layer in the colon was increased (P < 0·05) in rats fed C, P and RS when compared with rats fed a FF diet. In the colon, positive correlations were observed between the total thickness of the mucous layer and the area of neutral mucins, the pool of SCFA and the pool of acetic acid, while it was negatively correlated with the proportion of butyrate. The total thickness of the mucous layer was not correlated with the MUC gene transcription. The transcription of the gene MUC2 was negatively correlated (P = 0·04), whereas the transcription of MUC3 was positively correlated (P = 0·05) with the butyrate pool in the caecum. No correlations between the MUC2 or MUC3 transcription and SCFA were found in the colon. Hence, the regulation of the MUC genes differs between the compartments of the hindgut and, within compartments, the MUC genes may be regulated differently. In conclusion, a diet providing a large pool of SCFA with a low proportion of butyrate in the colon stimulates the formation of a thick mucous layer, which probably benefits intestinal health.

Soya isoflavones: genistein and daidzein are increasingly consumed in Western countries. Their beneficial effects are discussed considering nutrition and health in Asia. The present study aimed to check whether chronic ingestions, ethnic origin and dietary context can influence soya phyto-oestrogen bioavailability. Two prospective trials were carried out to blindly assess the pharmacokinetics after acute and chronic intake of soya-based cheese (45·97 (sd1·57) mg isoflavones) taken once a day for 10 d. Twelve healthy young Asians immersed for 2 months in France were randomised in a cross-over design to compare the influence of a Western v. Asian dietary context. The second trial partly nested in the first one, compared Asians under the Western diet to twelve healthy young male Caucasians under the same diet. All volunteers were non-equol producers. After an acute intake of soya in Western diet, Asians exhibited higher maximum concentration measured in plasma (Cmax) and area under the plasma concentration–time curve (AUC) for genistein and daidzein than Caucasians (P = 0·005, 0·006, 0·032 and 0·008, respectively). In Caucasians under Western diet, AUC and Cmax values significantly increased after chronic intake. This was not the case for daidzein in Asians whatever the dietary context. For the first time, it is evidenced that on acute intake of soya cheese, Asians absorb soya phyto-oestrogens better than Caucasians, regardless of whether the background diet is Western or Asian. On chronic ingestions, AUC and Cmax values were increased for daidzein and genistein in Caucasians but not in Asians. There are ethnical differences in isoflavone pharmacokinetic and bioavailability. This may influence health outcomes.

Mechanisms underlying the lipodystrophy syndrome associated with antiretroviral therapy (ART) for HIV infection are not completely understood. We investigated the effect of ART on blood lipid concentrations in the fasting state and after consumption of a meal containing [1-13C]palmitic acid in HIV-positive men receiving nucleoside reverse transcriptase inhibitors (NRTI, n 7), NRTI combined with protease inhibitors (PI; NRTIPI, n 6), in HIV-positive but therapy-naïve men (noART, n 5) and in HIV-seronegative men (controls, n 6). HIV-positive subjects had higher fasting TAG concentrations and resting energy expenditure than controls. Subjects receiving NRTIPI therapy had higher fasting NEFA concentrations than the other groups. There were no significant differences in postprandial lipid metabolism between noART subjects and controls. NRTI therapy impaired hydrolysis of meal-derived TAG, most evidently when combined with PI (the NRTIPI group). Accumulation of 13C-label in the NEFA fraction was not different between groups. In the NRTIPI group, fasting and postprandial NEFA concentrations were significantly higher than other groups. Postprandial glucose and insulin responses in HIV-positive subjects did not differ from controls. These findings suggest that ART dyslipidaemia is associated with impaired postprandial TAG clearance, which is exacerbated by NRTIPI therapy. If dyslipidaemia is to be minimised in ART, the specific adverse effects of particular combinations during the fed state should be considered.

The present study aimed at comparing the anthropometric profile of Asian Indian adolescents from Guadeloupe with that of their island counterparts. A total of 720 voluntary 11- to 17-year-old students participated: 180 Asian Indians and 540 age- and sex-matched students of other origin. Weight and height were measured to calculate the BMI. Waist and hip circumferences and bicipital, tricipital, subscapular and supra-iliac skinfold thicknesses were assessed. The percentage of body fat was estimated by bioelectrical impedance analysis. Obesity was defined from BMI according to the International Obesity Task Force recommendations. Asian Indians were smaller and lighter than their counterparts. They had a higher body fat percentage even after adjustment on BMI but the prevalence of obesity did not differ, with an overall prevalence of 5·69 (95 % CI 5·67, 5·71) %. No principal effects of ethnicity on waist and hip circumferences or the waist:hip ratio were evidenced. The sum of the four skinfold thicknesses was the strongest predictor of body fat percentage, and the adjustment of overall body fat on subcutaneous fat cancelled the effect of ethnicity on this dependent variable. The present study found that Asian Indian adolescents from Guadeloupe had the same tendency toward higher body fat and body fat-for-BMI as previously documented in Asian Indian adults. It raises the hypothesis of a higher cardiovascular risk in this ethnic group from adolescence and questions the validity of using common BMI references for screening obesity in multiethnic communities.

The Mini Nutritional Assessment (MNA) is recommended for grading nutritional status in the elderly. A new index for predicting the risk of nutrition-related complications, the Geriatric Nutritional Risk Index (GNRI), was recently proposed but little is known about its possible use in the assessment of nutritional status. Thus, we aimed to investigate its ability to assess the nutritional status and predict the outcome when compared with the MNA. Anthropometry and biochemical parameters were determined in 241 institutionalised elderly (ninety-four males and 147 females; aged 80·1 (sd 8·3) years). Nutritional risk and nutritional state were graded by the GNRI and MNA, respectively. At 6 months outcomes were: death; infections; bedsores. According to the GNRI and MNA, the prevalence of high risk (GNRI <  92)/malnutrition (MNA <  17), moderate risk (GNRI 92–98)/malnutrition at-risk (MNA 17–23·5) and no risk (GNRI > 98)/good status (MNA > 24) were 20·7/12·8 %, 36·1/39 % and 43·2/48·2 %, respectively, with poor agreement in scoring the patient (Cohen's kappa test: κ = 0·29; 95 % CI 0·19, 0·39). GNRI categories showed a stronger association (OR) with overall outcomes than MNA classes, although no difference (P>0·05) was found between malnutrition (v. ‘good status’, OR 6·4; 95 % CI 2·1, 71·9) and high nutritional risk (v. ‘no risk’, OR 9·7; 95 % CI 3·0, 130). Multivariate logistic regression revealed the GNRI as an independent predictor of complications. In overall-outcome prediction, a good sensitivity was found only for GNRI <  98 (0·86 (95 % CI 0·67, 0·96)). The combination of a GNRI > 98 with an MNA > 24 seemed to exclude adverse outcomes. The GNRI showed poor agreement with the MNA in nutritional assessment, but appeared to better predict outcome. In home-care resident elderly, outcome prediction should be performed by combining the suggestions from both these tools.

Excess calcium is well known to induce iron deficiency. Furthermore, excess calcium increases hepatic copper concentration and decreases renal copper concentration. We investigated the effect of iron supplementation on the tissue distribution of copper in rats given a high-calcium diet. Male rats (5 weeks old) were divided into four groups; a control group, and three groups given a diet containing 5-fold higher calcium than its requirement and an intraperitoneal iron supplementation of 0, 1 or 2 mg/week as iron dextran. The animals were fed their respective experimental diets with or without iron supplementation for 4 weeks. Although the high-calcium diet had no effect on calcium concentrations in the liver, kidney, testis, spleen and plasma, it reduced haematocrit and iron concentrations in the liver, kidney and testis and the rats had a moderate iron deficiency. The iron supplementation restored to normal these signs of iron deficiency. The high-calcium diet increased hepatic copper concentration but decreased plasma copper concentration and ceruloplasmin activity, which was restored by the iron supplementation. The copper concentration in bile was neither affected by the high-calcium diet nor the iron supplementation. The high-calcium diet decreased the copper concentration in the kidney, which was not restored by the iron supplementation. These results suggest that secondary iron deficiency stimulates hepatic accumulation of copper in rats given excess calcium by suppressing copper efflux into the circulation. The reduced renal copper concentration by excess calcium is independent of the iron deficiency.

The objective of the present study was to determine the potential long-term impact of dietary habits on age-related decline among 4809 elderly women (born between 1925 and 1930) in the ‘Etude Epidémiologique de Femmes de la Mutuelle Générale de l'Education Nationale’ (E3N) study, a French epidemiological cohort. In 1993, an extensive diet history self-administered questionnaire was sent to all participants, and in 2006 another questionnaire on instrumental activities of daily living (IADL) and recent cognitive change was sent to a close relative or friend of each woman. Logistic models adjusted for socio-demographic, lifestyle and health factors were performed to evaluate associations between habitual dietary intakes and two outcomes of interest based on the informant response: recent cognitive decline and IADL impairment. Recent cognitive decline was associated with lower intakes of poultry, fish, and animal fats, as well as higher intakes of dairy desserts and ice-cream. IADL impairment was associated with a lower intake of vegetables. The odds of recent cognitive decline increased significantly with decreasing intake of soluble dietary fibre and n-3 fatty acids but with increasing intake of retinol. The odds of IADL impairment increased significantly with decreasing intakes of vitamins B2, B6 and B12. These results are consistent with a possible long-term neuroprotective effect of dietary fibre, n-3 polyunsaturated fats and B-group vitamins, and support dietary intervention to prevent cognitive decline.

Studies of the beneficial role of fish consumption in the prevention of CVD are not consistent in their findings, particularly those studies that focus on the risk of stroke. The aim of the present study is to investigate the relationship between the consumption of different types of fish and the subsequent incidence of cerebrovascular disease (CVA). We prospectively evaluated the association between consumption of different types of fish and CVA in 3958 men and women aged 40–79 years who were free of heart disease and had participated in a health examination survey from 1967 to 1972. A total of 659 incident cases of CVA occurred during a follow-up until the end of 1994. A dietary history interview method provided data on habitual consumption of fish and other foods over the preceding year at baseline. Total fish intake did not predict CVA, but consumption of salted fish suggested an increased risk of intracerebral haemorrhage. The relative risk of intracerebral haemorrhage between the highest tertile of salted fish consumption and non-consumers was 1·98 (95 % CI 1·02, 3·84; P for trend = 0·06) after adjustment for age, sex, energy intake, smoking, BMI, physical activity, geographic area, occupation, diabetes, use of post-menopausal hormones, serum cholesterol, hypertension, and consumptions of butter, vegetables, fruits and berries. The relationship between fish consumption and stroke risk is not straightforward. How the fish is prepared for consumption may play an important role, affecting the association.

Previous studies have indicated low serum carotenoid concentrations among cigarette smokers and/or alcohol drinkers, but little is known about the interaction of smoking and drinking with serum carotenoids. We tested the hypothesis that smoking and drinking reduce serum carotenoid concentrations synergistically. A total of 1073 subjects (357 male and 716 female) who had received health examinations in the town of Mikkabi, Shizuoka Prefecture, Japan, participated in the study. The subjects were divided into six groups according to alcohol intake (non-drinkers, < 1 g/d; light drinkers, ≥ 1, < 25 g/d; moderate-to-heavy drinkers, ≥ 25 g/d) and smoking status (non-smokers and current smokers). The dietary intakes and serum concentrations of six carotenoids (lycopene, α-carotene, β-carotene, lutein, β-cryptoxanthin and zeaxanthin) within each group were evaluated cross-sectionally. The dietary intakes of all carotenoids did not differ in the six groups after adjusting for age and sex. The multivariate-adjusted means of the serum carotenoid concentrations in non-drinkers did not differ between non-smokers and current smokers. In contrast, the adjusted means of serum α-carotene, β-carotene and β-cryptoxanthin were significantly lower than those with increased alcohol intake, and these lower serum carotenoids among alcohol drinkers were more evident in current smokers than in non-smokers. Serum lycopene of moderate-to-heavy drinkers was significantly lower than that of non-drinkers, but it was not influenced by smoking. Neither smoking nor drinking was associated with the serum concentrations of lutein and zeaxanthin. These results suggest that smoking and drinking may reduce the serum α-carotene, β-carotene and β-cryptoxanthin concentrations in a synergistic manner.

Studies that have investigated ascorbic acid (AA) concentrations in cord blood have pointed to significant associations with maternal blood AA concentrations, smoking, age, diet, type of delivery, duration of gestation, fetal distress and birth weight. The aim of the present study was to determine the relationship between cord blood AA concentrations in newborns and maternal characteristics. A total of 117 Brazilian healthy parturients were included in this cross-sectional study. The concentrations of AA in blood were determined by the HPLC method. Data concerning socio-economic, demographic, obstetric, nutritional and health characteristics of the parturients, including alcohol consumption and smoking habit, were assessed by a standardised questionnaire. A FFQ was used to investigate the intake of foods rich in vitamin C. Cord blood AA concentration was significantly correlated with per capita income (r 0·26; P = 0·005), maternal blood AA concentration (r 0·48; P < 0·001) and maternal vitamin C-rich food intake score (r 0·36; P < 0·001). The linear regression model including maternal AA concentration, alcohol consumption, smoking, parity, vitamin C-rich food intake score and per capita income explained 31·13 % of the variation in cord blood AA concentrations in newborns. We recommend further experimental studies to assess the effects of ethanol on placental AA uptake, and epidemiological cohort studies to evaluate in detail the influence of maternal alcohol consumption on cord blood AA concentrations.

Females perform better in certain memory-related tasks than males. Sex differences in cognitive performance may be attributable to differences in circulating oestrogen acting on oestrogen β receptors (ERβ) which are prevalent in brain regions such as the hippocampus, frontal lobe and cortex that mediate cognitive functions. Since soya isoflavones are known to activate ERβ, chronic isoflavone supplementation in males may improve cognitive performance in memory-related tasks. A 12-week double-blind, placebo-controlled cross-over trial was conducted in thirty-four healthy men to investigate the effect of isoflavone supplementation on cognitive function. Volunteers were randomised to take four capsules/d containing soya isoflavones (116 mg isoflavone equivalents/d: 68 mg daidzein, 12 mg genistein, 36 mg glycitin) or placebo for 6 weeks, and the alternate treatment during the following 6 weeks. Assessments of memory (verbal episodic, auditory and working), executive function (planning, attention, mental flexibility) and visual-spatial processing were performed at baseline and after each treatment period. Isoflavone supplementation significantly improved spatial working memory (P = 0·01), a test in which females consistently perform better than males. Compared with placebo supplementation, there were 18 % fewer attempts (P = 0·01), 23 % fewer errors (P = 0·02) and 17 % less time (P = 0·03) required to correctly identify the requisite information. Isoflavones did not affect auditory and episodic memory (Paired Associate Learning, Rey's Auditory Verbal Learning Task, Backward Digit Span and Letter-Number Sequencing), executive function (Trail Making and Initial Letter Fluency Task) or visual-spatial processing (Mental Rotation Task). Isoflavone supplementation in healthy males may enhance cognitive processes which appear dependent on oestrogen activation.

There are multiple lines of evidence that lactic acid bacteria (LAB) exert cancer-preventive effects. However, the underlying mechanisms are poorly understood. In the present study we found that the cytoplasmic fraction of Lactococcus lactis ssp. lactis American Type Culture Collection (ATCC) 7962 exerted the strongest antiproliferative effects (half-maximal inhibitory concentration (IC50) = 17 μg/ml) in SNU-1 human stomach cancer cells and arginine deiminase (ADI; EC 3.5.3.6) activity. We also cloned, expressed and purified ADI from L. lactis ssp. lactis ATCC 7962 (LADI). Both purified ADI from L. lactis (PADI; IC50 = 2 μg/ml) and recombinant ADI originating from LADI (IC50 = 0·6 μg/ml) inhibited the proliferation of SNU-1 cells. LADI induced G0/G1-phase arrest, sub-G1 accumulation, DNA condensation and DNA fragmentation in SNU-1 cells. 4′,6-Diamidino-2-phenylindole (DAPI) staining and DNA fragmentation data provide evidence that LADI induces apoptosis in SNU-1 cells. LADI increased the expressions of p53 and p27Kip1, and decreased the expressions of cyclin D1, c-myc and Bcl-xL in SNU-1 cells. However, LADI had no effects on the expressions of p21Cip1 and Bcl-2. Collectively, these data indicate that ADI induces apoptosis and G0/G1-phase arrest of SNU-1 cells, which might contribute to the chemopreventive potential of LAB.

Excessive gestational weight gain and postpartum weight retention are risk factors for female obesity. The present study was to examine dietary intakes and weight history from a prospective follow-up study from early pregnancy to 1 year postpartum. A total of 151 pregnant women within 20 weeks of pregnancy in Taipei, Taiwan were interviewed periodically to collect dietary and lifestyle information. The participants had an average age of 30 years and the average gestational weight gain was 14 kg, with an average daily intake of 7830 kJ (1870 kcal) in the 1 year following parturition. By bivariate analyses, maternal age, pre-pregnancy BMI and breast-feeding were not related to postpartum weight retention, but gestational weight gain had significant positive correlations (r 0·54 at 6 months, r 0·44 at 1 year; P < 0·05). The generalised estimating equations showed that the average weight before pregnancy, at 6 months and 1 year postpartum was 53·35 kg, 55·75 kg (weight retention 2·36 kg; P < 0·01) and 54·75 kg (weight retention 1·48 kg; P < 0·01), respectively. After controlling for age, pre-pregnancy BMI, gestational weight gain and parity, we found at 6 months that the adjusted weight retention at postpartum was 0·79 kg (P < 0·01), but at 1 year it was − 0·08 kg (P>0·05). From multivariate analyses, dietary energy intake and energy intake per kg body weight as a long-term physical activity index could explain 24 % of the variation at 6 months and 27 % of the variation at 1 year in postpartum weight retention. These results suggest that pregnant women should be advised to control gestational weight gain, decrease energy intakes after child-bearing and maintain regular exercise in order to prevent postpartum obesity.

The salt content of processed foods is important because of the high intake of Na by most New Zealanders. A database of Na concentrations in fifty-eight processed foods was compiled from existing and new data and combined with 24 h diet recall data from two national nutrition surveys (5771 respondents) to derive salt intakes for seven population groups. Mean salt intakes from processed foods ranged from 6·9 g/d for young males aged 19–24 years to 3·5 g/d for children aged 5–6 years. A total of  ≥ 50 % of children aged 5–6 years, boys aged 11–14 years and young males aged 19–24 years had salt intakes that exceeded the upper limit for Na, calculated as salt (3·2–5·3 g/d), from processed foods only. Bread accounted for the greatest contribution to salt intake for each population group (35–43 % of total salt intake). Other foods that contributed 2 % or more and common across most age groups were sausage, meat pies, pizza, instant noodles and cheese. The Na concentrations of key foods have changed little over the 16-year period from 1987 to 2003 except for corned beef and whole milk that have decreased by 34 and 50 % respectively. Bread is an obvious target for salt reduction but the implication on iodine intake needs consideration as salt is used as a vehicle for iodine fortification of bread.